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o fp e o p l e( 3 ) .C o m p a r e dw i t hF P Ga n dA 1 C\nc u tp o i n t s ,t h e2 - hP Gv a l u ed i a g n o s e sm o r epeople with prediabetes and diabetes (4).Moreover, the effi cacy of interventions for | [
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primary prevention of type 2 diabetes hasmainly been demonstrated among individu-als who have impaired glucose tolerance(IGT) with or without elevated fasting glu-cose, not for individuals with isolated im-paired fasting glucose (IFG) or for those withprediabetes de fined by A1C criteria (5 –8).\nT h es a m et e s t sm ... | [
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T h es a m et e s t sm a yb eu s e dt os c r e e n\nfor and diagnose diabetes and to detect in-dividuals with prediabetes (9) (Table 2.1andTable 2.2 ). Diabetes may be identi fied\nanywhere along the spectrum of clinical\nscenarios— in seemingly low-risk individuals\nwho happen to have glucose testing, in indi- | [
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who happen to have glucose testing, in indi-\nviduals screened based on diabetes risk as-sessment, and in symptomatic individuals.There is presently insuf ficient evidence to\nsupport the use of continuous glucose mon-itoring (CGM) for screening or diagnosisof prediabetes or diabetes. For additionaldetails on the eviden... | [
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the criteria for the diagnosis of diabetes,\nprediabetes, and abnormal glucose toler-\nance (IFG and IGT), see the American Diabe-tes Asso-ciation (ADA) position statement\n“Diagnosis and Classi fication of Diabetes\nMellitus” (2) and other reports (3,10,11).\nUse of Fasting Plasma Glucose or\n2-Hour Plasma Glucose for ... | [
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2-Hour Plasma Glucose for Screeningand Diagnosis of Diabetes\nIn the less common clinical scenario where\na person has classic hyperglycemic symp-toms (e.g., polyuria, polydipsia, and unex-\nplained weight loss), measurement of\nrandom plasma glucose is suf ficient to diag-\nnose diabetes (symptoms of hyperglycemia | [
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nose diabetes (symptoms of hyperglycemia\nor hyperglycemic crisis plus random plasma\nglucose $200 mg/dL [ $11.1 mmol/L]). In\nt h e s ec a s e s ,k n o w i n gt h ep l a s m ag l u c o s e\nlevel is critical because, in addition to con-\nfirming that symptoms are due to diabe-\ntes, it will inform management decisions. | [
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tes, it will inform management decisions.\nHealth care professionals may also wantto know the A1C to determine the chro-\nnicity of hyperglycemia.\nIn an individual without symptoms, FPG\nor 2-h PG can be used for screening and di-\nagnosis of diabetes. In nonpregnant individ- | [
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agnosis of diabetes. In nonpregnant individ-\nuals, FPG (or A1C) is typically preferred forroutine screening due to the ease of admin-\nistration; however, the 2-h PG (OGTT) test-\ning protocol may identify individuals withdiabetes who may otherwise be missed\n(e.g., those with cystic fibrosis –related\ndiabetes or post... | [
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diabetes or posttransplantation diabe-\ntes mellitus). In the absence of classic\nhyperglycemic symptoms, repeat test-\ning is required to con firm the diagnosis\nregardless of the test used (see\nCONFIRMING\nTHE DIAGNOSIS , below).\nAn advantage of glucose testing is that\nthese assays are inexpensive and widelyavailab... | [
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diurnal variation in glucose and fasting re-\nquirement. Individuals may have dif ficulty\nfasting for the full 8-h period or may mis-\nreport their fasting status. Recent physical\nactivity, illness, or acute stress can also af-fect glucose concentrations. Glycolysis is\nalso an important and underrecognized | [
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also an important and underrecognized\nc o n c e r nw i t hg l u c o s et e s t i n g .G l u c o s econcentrations will be falsely low if sam-\nples are not processed promptly or stored\nproperly prior to analysis (1).\nPeople should consume a mixed diet\nwith at least 150 g of carbohydrates on\nthe 3 days prior to OGT... | [
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the 3 days prior to OGTT (12 –14). Fasting\nand carbohydrate restriction can falsely\nelevate glucose level with an oral glucose\nchallenge.\nUse of A1C for Screening and\nDiagnosis of Diabetes\nRecommendations\n2.2a The A1C test should be performed\nusing a method that is certifi ed by the\nNational Glycohemoglobin Sta... | [
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National Glycohemoglobin Standardiza-\ntion Program (NGSP) as traceable to theDiabetes Control and Complications Trial\n(DCCT) reference assay. B\n2.2b Point-of-care A1C testing for dia-\nbetes screening and diagnosis should\nbe restricted to U.S. Food and DrugAdministration –approved devices at | [
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Clinical Laboratory Improvement Am-endments (CLIA) –certified laboratories\nthat perform testing of moderate com-\nplexity or higher by trained personnel. B\n2.3 Marked discordance between\nA1C and repeat blood glucose values | [
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2.3 Marked discordance between\nA1C and repeat blood glucose values\nshould raise the possibility of a problemor interference with either test. BTable 2.1 —Criteria for the diagnosis of diabetes in nonpregnant individuals\nA1C$6.5% ($48 mmol/mol). The test should be performed in a laboratory using a method | [
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that is NGSP certi fied and standardized to the DCCT assay.*\nOR\nFPG$126 mg/dL ( $7.0 mmol/L). Fasting is de fined as no caloric intake for at least 8 h.*\nOR\n2-h PG $200 mg/dL ( $11.1 mmol/L) during OGTT. The test should be performed as\ndescribed by the WHO, using a glucose load containing the equivalent of 75 g anhy... | [
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glucose dissolved in water.*\nOR\nIn an individual with classic symptoms of hyperglycemia or hyperglycemic crisis, a random\nplasma glucose $200 mg/dL ( $11.1 mmol/L). Random is any time of the day without\nregard to time since previous meal. | [
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regard to time since previous meal.\nDCCT, Diabetes Control and Complications Trial; FPG, fasting plasma glucose; OGTT, oral glu-cose tolerance test; NGSP, National Glycohemoglobin Standardization Program; WHO, World\nHealth Organization; 2-h PG, 2-h plasma glucose. *In the absence of unequivocal hypergly- | [
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cemia, diagnosis requires two abnormal test results obtained at the same time (e.g., A1Cand FPG) or at two different time points.\nTable 2.2 —Criteria de fining prediabetes in nonpregnant individuals\nA1C 5.7 –6.4% (39 –47 mmol/mol)\nOR\nFPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) (IFG)\nOR | [
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OR\nFPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) (IFG)\nOR\n2-h PG during 75-g OGTT 140 mg/dL (7.8 mmol/L) to 199 mg/dL (11.0 mmol/L) (IGT)\nFor all three tests, risk is continuous, extending below the lower limit of the range and becoming\ndisproportionately greater at the higher end of the range. FPG, fasting... | [
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paired fasting glucose; IGT, impaired glucose tolerance; OGTT, oral glucose tolerance test; 2-h PG,2-h plasma glucose.diabetesjournals.org/care Diagnosis and Classification of Diabetes S21\n©AmericanDiabetesAssociation | [
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2.4 In conditions associated with an\naltered relationship between A1C and\nglycemia, such as some hemoglobin var-\niants, pregnancy (second and third tri-mesters and the postpartum period),\nglucose-6-phosphate dehydrogenase de-\nficiency, HIV, hemodialysis, recent blood | [
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ficiency, HIV, hemodialysis, recent blood\nloss or transfusion, or erythropoietintherapy, plasma glucose criteria shouldbe used to diagnose diabetes. B\nThe A1C test should be performed using a\nmethod that is certifi ed by the National\nGlycohemoglobin Standardization Pro-gram (NGSP) (ngsp.org) and standardized\nor trac... | [
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or traceable to the Diabetes Control and\nComplications Trial (DCCT) reference as-say. Point-of-care A1C assays may beNGSP certi fied and cleared by the U.S.\nFood and Drug Administration (FDA) for\nuse in monitoring glycemic control in | [
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use in monitoring glycemic control in\npeople with diabetes in both ClinicalLaboratory Improvement Amendments(CLIA) –r e g u l a t e da n dC L I A - w a i v e ds e t t i n g s .\nFDA-approved point-of-care A1C testingcan be used in laboratories or sites thatare CLIA certi fied, are inspected, and meet | [
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the CLIA quality standards. These stand-ards include speci fied personnel require-\nments (including documented annualcompetency assessments) and participa-tion three times per year in an approvedproficiency testing program (15 –18).\nA1C has several advantages compared\nwith FPG and OGTT, including greater conve- | [
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with FPG and OGTT, including greater conve-\nnience (fasting not required), greater pre-\nanalytical stability, and fewer day-to-dayperturbations during stress, changes in nutri-tion, or illness. However, it should be notedthat there is lower sensitivity of A1C at the\ndesignated cut point compared with that of | [
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designated cut point compared with that of\nglucose tests as well as greater cost andlimited access in some parts of the world.\nA1C re flects glucose bound to hemo-\nglobin over the life span of the erythro-cyte (/C24120 days) and is thus a “weighted ” | [
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average that is more heavily affected byrecent blood glucose exposure. Thismeans that clinically meaningful changesin A1C can be seen in <120 days. A1C is\nan indirect measure of glucose exposure,\nand factors that affect hemoglobin con- | [
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and factors that affect hemoglobin con-\ncentrations or erythrocyte turnover canaffect A1C (e.g., thalassemia or folatedeficiency). A1C may not be a suitable\ndiagnostic test in people with anemia, peo-\nple treated with erythropoietin, or people | [
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ple treated with erythropoietin, or people\nundergoing hemodialysis or HIV treatment(19,20). Some hemoglobin variants caninterfere with A1C test results, but this de-\npends on the speci fic assay. For individuals\nwith a hemoglobin variant but normal red | [
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0.024390215054154396,
0.03887345641851425,
-0.0322067029774189,
0.029569052159786224,
-0.0777050256729126,
0.003630... |
with a hemoglobin variant but normal red\nblood cell turnover, such as those with thesickle cell trait, an A1C assay without inter-ference from hemoglobin variants should\nbe used. An updated list of A1C assays | [
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0.010481499135494232,
0.0011837572092190385,
-0.016012705862522125,
-0.10110004246234894,
... |
be used. An updated list of A1C assays\nwith interferences is available at ngsp.org/interf.asp. Another genetic variant,X-linked glucose-6-phosphate dehydroge-nase G202A, carried by 11% of AfricanAmerican individuals in the U.S., is associ-\nated with a decrease in A1C of about 0.8% | [
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ated with a decrease in A1C of about 0.8%\nin homozygous men and 0.7% in homozy-gous women compared with levels in indi-viduals without the variant (21).\nThere is controversy regarding racial dif-\nferences in A1C. Studies have found thatAfrican American individuals have slightly\nhigher A1C levels than non-Hispanic W... | [
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higher A1C levels than non-Hispanic White\nor Hispanic people (22 –25). The glucose-in-\ndependent racial difference in A1C is small(/C240.3 percentage points) and may re flect\ngenetic differences in hemoglobin or red\ncell turnover that vary by ancestry. There is\nan emerging understanding of the geneticdeterminants o... | [
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adequate genetic data in diverse popula-tions (26,27). While some genetic variantsmight be more common in certain race or\nancestry groups, it is important that we do | [
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ancestry groups, it is important that we do\nnot use race or ancestry as proxies forpoorly understood genetic differences. Re-assuringly, studies have shown that the as-sociation of A1C with risk for complicationsappears to be similar in African American\nand non-Hispanic White populations (28).\nConfirming the Diagnos... | [
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and non-Hispanic White populations (28).\nConfirming the Diagnosis\nUnless there is a clear clinical diagnosis\n(e.g., individual with classic symptomsof hyperglycemia or hyperglycemic crisisand random plasma glucose $200 mg/dL\n[$11.1 mmol/L]), diagnosis requires two ab- | [
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[$11.1 mmol/L]), diagnosis requires two ab-\nnormal screening test results, measured ei-t h e ra tt h es a m et i m e( 2 9 )o ra tt w odifferent time points. If using samples at twodifferent time points, it is recommendedthat the second test, which may be either arepeat of the initial test or a different test, | [
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be performed promptly. For example, if the\nA1C is 7.0% (53 mmol/mol) and a repeat re-sult is 6.8% (51 mmol/mol), the diagnosis ofdiabetes is con firmed. Two different tests\n( s u c ha sA 1 Ca n dF P G )b o t hh a v i n gr e s u l t sabove the diagnostic threshold when\ncollected at the same time or at two dif- | [
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0... |
collected at the same time or at two dif-\nferent time points would also con firm the di-\nagnosis. On the other hand, if an individualhas discordant results from two differenttests, then the test result that is above thediagnostic cut point should be repeated,with careful consideration of factors that\nmay affect measu... | [
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may affect measured A1C or glucose levels.\nThe diagnosis is made based on the con fir-\nmatory screening test. For example, if an in-dividual meets the diabetes criterion of A1C\n(two results $6.5% [ $48 mmol/mol]) but\nnot FPG ( <126 mg/dL [ <7.0 mmol/L]), that\nperson should nevertheless be considered\nto have diabet... | [
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person should nevertheless be considered\nto have diabetes.\nIf individuals have test results near\nthe margins of the diagnostic threshold,the health care professional should edu-cate the individual about the onset of\npossible hyperglycemic symptoms and\nrepeat the test in 3 –6m o n t h s .\nConsistent and substantia... | [
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Consistent and substantial discordance\nbetween glucose and A1C test results shouldprompt additional follow-up to determine\nthe underlying reason for the discrepancy\nand whether it has clinical implications forthe individual. In addition, consider other bi-\nomarkers, such as fructosamine and glycated | [
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omarkers, such as fructosamine and glycated\nalbumin, which are alternative measures ofchronic hyperglycemia that are approved forclinical use for monitoring glycemic control in\npeople with diabetes.\nCLASSIFICATION\nRecommendation\n2.5Classify people with hyperglycemia\ninto appropriate diagnostic catego-\nries to ai... | [
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ries to aid in personalized manage-ment. E\nDiabetes is classi fied conventionally into\nseveral clinical categories, although\nthese are being reconsidered based on\ngenetic, metabolomic, and other charac-\nteristics and pathophysiology (2):\n1. Type 1 diabetes (due to autoimmune\nb-cell destruction, usually leading to | [
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0.02378706820309162,
-0.08475998044013977,
-0.0017... |
b-cell destruction, usually leading to\nabsolute insulin de ficiency, including\nlatent autoimmune diabetes in adults)\n2. Type 2 diabetes (due to a non-autoim-\nmune progressive loss of adequate\nb-cell insulin secretion, frequently on\nthe background of insulin resistance\nand metabolic syndrome)\n3. Speci fic types of... | [
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and metabolic syndrome)\n3. Speci fic types of diabetes due to\nother causes, e.g., monogenic dia-\nbetes syndromes (such as neonatal\ndiabetes and maturity-onset diabetes of\nthe young), diseases of the exocrineS22 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDi... | [
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pancreas (such as cystic fibrosis and\npancreatitis), and drug- or chemical-in-\nduced diabetes (such as with glucocorti-\ncoid use, in the treatment of people\nwith HIV, or after organ transplantation)\n4. Gestational diabetes mellitus (diabe-\ntes diagnosed in the second or thirdtrimester of pregnancy that was notclea... | [
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tion or other types of diabetes occur-\nring throughout pregnancy, such as\ntype 1 diabetes).\nThis section reviews most common forms\nof diabetes but is not comprehensive. For\nadditional information, see the ADA posi-\ntion statement “Diagnosis and Classi fica-\ntion of Diabetes Mellitus ”(2). | [
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0.0... |
tion of Diabetes Mellitus ”(2).\nType 1 diabetes and type 2 diabetes areheterogeneous diseases in which clinical\npresentation and disease progression may\nvary considerably. Classifi cation is impor-\ntant for determining personalized therapy,\nbut some individuals cannot be clearly\nclassified as having type 1 or type ... | [
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classified as having type 1 or type 2 diabe-\ntes at the time of diagnosis. The traditionalparadigms of type 2 diabetes occurring\nonly in adults and type 1 diabetes only in\nchildren are not accurate, as both diseasesoccur in all age-groups. Children with type 1\ndiabetes often present with the hallmark\nsymptoms of po... | [
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symptoms of polyuria/polydipsia, and ap-\nproximately half present with diabetic\nketoacidosis (DKA) (30 –32). The onset of\ntype 1 diabetes may be more variable inadults; they may not present with the classic\nsymptoms seen in children and may experi-\nence temporary remission from the needfor anticipated full-dose in... | [
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(33–35). The features most useful in discrim-\nination of type 1 diabetes include youngerage at diagnosis ( <35 years) with lower\nBMI (<25 kg/m\n2), unintentional weight\nloss, ketoacidosis, and plasma glucose\n>360 mg/dL ( >20 mmol/L) at presenta-\ntion (36) ( Fig. 2.1 ). Other features classi- | [
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0.0... |
tion (36) ( Fig. 2.1 ). Other features classi-\ncally associated with type 1 diabetes,such as ketosis without acidosis, osmotic\nsymptoms, family history, or a history of\nautoimmune diseases, are weak discrim-\ninators. Occasionally, people with type 2\ndiabetes may present with DKA (37,38), par-ticularly members of c... | [
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0.03248... |
nic groups (e.g., African American adults,\nwho may present with ketosis-prone type 2\ndiabetes) (39).\nIt is important for health care professio-\nnals to realize that classi fication of diabetes\ntype is not always straightforward atpresentation and that misdiagnosis is com-\nm o na n dc a no c c u ri n /C2440% of adu... | [
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m o na n dc a no c c u ri n /C2440% of adults with\nnew type 1 diabetes (e.g., adults with type1 diabetes misdiagnosed as having type 2\ndiabetes and individuals with maturity-onset diabetes of the young [MODY] mis-\ndiagnosed as having type 1 diabetes)\n(36). Although dif ficulties in distinguish-\ning diabetes type ma... | [
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0.027046... |
ing diabetes type may occur in all age-\ngroups at onset, the diagnosis becomes\nmore obvious over time in people withb-cell de ficiency as the degree of b-cell\ndeficiency becomes clear ( Fig. 2.1). One\nuseful clinical tool for distinguishing dia-\nbetes type is the AABBCC approach: Age\n(e.g., for individuals <35 year... | [
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-0.04126744717359543,
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(e.g., for individuals <35 years old, consider\ntype 1 diabetes); Autoimmunity (e.g., per-sonal or family history of autoimmune\ndisease or polyglandular autoimmune syn-dromes); Body habitus (e.g., BMI <25 kg/m\n2);\nBackground (e.g., family history of type 1diabetes); Control (e.g., level of glucosecontrol on noninsul... | [
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0.01... |
morbidities (e.g., treatment with immune\ncheckpoint inhibitors for cancer can causeacute autoimmune type 1 diabetes)\n(36).\nIn both type 1 and type 2 diabetes, ge-\nnetic and environmental factors can re-\nsult in the progressive loss of b-cell mass | [
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sult in the progressive loss of b-cell mass\nand/or function that manifests clinicallyas hyperglycemia. Once hyperglycemiaoccurs, people with all forms of diabetes\nare at risk for developing the same\nchronic complications, although rates of\nprogression may differ. The identi fication\nof individualized therapies for ... | [
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of individualized therapies for diabetes\nin the future will be informed by better\ncharacterization of the many paths to\nb-cell demise or dysfunction (40). Across\nthe globe, many groups are working on\ncombining clinical, pathophysiological, and\ngenetic characteristics to more precisely\ndefine the subsets of diabet... | [
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0.01... |
define the subsets of diabetes that are cur-\nrently clustered into the type 1 diabetes\nversus type 2 diabetes nomenclature with\nthe goal of optimizing personalized treat-\nment approaches (41).\nCharacterization of the underlying\npathophysiology is more precisely devel-\noped in type 1 diabetes than in type 2 di- | [
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0.0008419051300734282,
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0.0625011995434761,
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oped in type 1 diabetes than in type 2 di-\nabetes. It is clear from prospective stud-\nies that the persistent presence of two\nor more islet autoantibodies is a near-certain predictor of clinical diabetes (42).\nIn at-risk cohorts followed from birth or a\nvery young age, seroconversion rarely oc-curs before 6 months... | [
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0.02963465079665184,
-0.09672354906797409,
0.027536... |
a peak in seroconversion between 9 and24 months of age (43 –45). The rate of\nprogression is dependent on the age at\nfirst detection of autoantibody, number of\nautoantibodies, autoantibody speci ficity, and\nautoantibody titer. Glucose and A1C levels\nmay rise well before the clinical onset of | [
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0.15167249739170074,
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0.03491635248064995,
-0.03044503554701805,
-0.035686664283275604,
0.0... |
may rise well before the clinical onset of\ndiabetes (e.g., changes in FPG and 2-h PGcan occur about 6 months before diagno-\nsis) (46), making diagnosis feasible well\nbefore the onset of DKA. Three distinct\nstages of type 1 diabetes have been de-\nfined ( Table 2.3 ) and serve as a frame-\nwork for research and regul... | [
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work for research and regulatory decision-\nmaking (40,47).\nThere is debate as to whether slowly\nprogressive autoimmune diabetes withan adult onset should be termed latent\nautoimmune diabetes in adults (LADA) ortype 1 diabetes. The clinical priority with\ndetection of LADA is awareness that slow\nautoimmune b-cell d... | [
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autoimmune b-cell destruction can occur\nin adults, leading to a long duration ofmarginal insulin secretory capacity. For\nthis classi fication, all forms of diabetes\nmediated by autoimmune b-cell destruc-\ntion independent of age of onset areincluded under the rubric of type 1 dia-\nbetes. Use of the term LADA is comm... | [
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betes. Use of the term LADA is common\nand acceptable in clinical practice and has\nthe practical impact of heightening aware-ness of a population of adults likely to\nhave progressive autoimmune b-cell de-\nstruction (48), thus accelerating insulin ini-tiation prior to deterioration of glucose | [
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management or development of DKA( 3 4 , 4 9 ) .A tt h es a m et i m e ,t h e r ei se v i -\ndence that application of only a single im-\nperfect autoantibody test for determining\nLADA classi fication may lead to misclassi-\nfication of some individuals with type 2\ndiabetes. Diagnostic accuracy may be\nimproved by utili... | [
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0.0662... |
improved by utilizing higher-speci ficity\ntests, con firmatory testing for other auto-\nantibodies, and restricting testing to thosewith clinical features suggestive of autoim-\nmune diabetes (50).\nThe paths to b-cell demise and dysfunc-\ntion are less well defi n e di nt y p e2d i a b e -\ntes, but de ficient b-cell ins... | [
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0.0147480... |
tes, but de ficient b-cell insulin secretion,\nfrequently in the setting of insulin resistance,\nappears to be the common denominator.\nType 2 diabetes is associated with insulin\nsecretory defects related to genetic predis-position, epigenetic changes, infl ammation,\nand metabolic stress. Future classifi cation\nschemes... | [
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schemes for diabetes will likely focus on\nthe pathophysiology of the underlying\nb-cell dysfunction (40,51 –54).diabetesjournals.org/care Diagnosis and Classification of Diabetes S23\n©AmericanDiabetesAssociation | [
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TYPE 1 DIABETES\nRecommendations\n2.6Screening for presymptomatic type 1\ndiabetes may be done by detection of\nautoantibodies to insulin, glutamic acid\ndecarboxylase (GAD), islet antigen 2\n(IA-2), or zinc transporter 8 (ZnT8). B\n2.7 Having multiple con firmed islet | [
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0.11461074650287628,
0.06560951471328735,
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0.... |
2.7 Having multiple con firmed islet\nautoantibodies is a risk factor for clini-cal diabetes. Testing for dysglycemiamay be used to further forecast near-\nterm risk. When multiple islet autoanti-\nbodies are identi fied, referral to a spe-\ncialized center for further evaluationand/or consideration of a clinical trial | [
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0.11272988468408585,
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0.0005330454441718757,
0.004088615998625755,
-0.04733353853225708,
-0.06673672795295715,
0.... |
or approved therapy to potentially de-\nlay development of clinical diabetes\nshould be considered. B\n2.8 Standardized islet autoantibody\ntests are recommended for classi fica-\ntion of diabetes in adults who havephenotypic risk factors that overlap\nwith those for type 1 diabetes (e.g.,\nyounger age at diagnosis, uni... | [
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0.06746379286050797,
0.06253960728645325,
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0.0009739879169501364,
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0.043728433549404144,
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0.... |
younger age at diagnosis, unintentional\nweight loss, ketoacidosis, or short time\nto insulin treatment). E\nImmune-Mediated Diabetes\nAutoimmune type 1 diabetes accounts for\n5–10% of diabetes and is caused by auto-\nimmune destruction of the pancreatic\nb-cells. Autoimmune markers include islet\ncell autoantibodies a... | [
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0.13598446547985077,
0.10115526616573334,
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0.007781652268022299,
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-0.048864349722862244,
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0.0... |
cell autoantibodies and autoantibodies to\nglutamic acid decarboxylase (GAD) (suchas GAD65), insulin, the tyrosine phospha-tases islet antigen 2 (IA-2) and IA-2 b,a n d\nzinc transporter 8 (ZnT8). Numerous clini-\ncal studies are being conducted to test | [
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-0.008220006711781025,
0.14602148532867432,
0.05729474127292633,
0.012110873125493526,
0.053231481462717056,
0.005159992258995771,
-0.007121427915990353,
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0.09... |
cal studies are being conducted to test\nvarious methods of preventing or delayingtype 1 diabetes in those with evidence ofislet autoimmunity (trialnet.org/our-research/prevention-studies) (42 –44,49,55,56). The\ndisease has strong HLA associations, with\nlinkage to the DQB1 and DRB1 haplo- | [
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0.05973242595791817,
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0.07183955609798431,
0.04457109421491623,
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0.03103511966764927,
-0.06745895743370056,
0.015... |
linkage to the DQB1 and DRB1 haplo-\ntypes, and genetic screening has beenused in some research studies to identifyhigh-risk populations. Speci fic alleles in\nthese genes can be either predisposing(e.g., DRB1*0301-DQB1*0201 [DR3-DQ2]and DRB1*0401-DQB1*0302 [DR4-DQ8])or protective (e.g., DRB1*1501 and DQA1*\n0102-DQB1*0... | [
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0.033312954008579254,
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0.08182267844676971,
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0.04894706606864929,
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-0.0... |
0102-DQB1*0602). Stage 1 of type 1 diabe-\ntes is de fined by the presence of two or\nmore of these autoantibodies and normo-glycemia. At stage 1, the 5-year risk of de-veloping symptomatic type 1 diabetes is/C2444% overall but varies considerably\nbased on number, titer, and speci ficity of | [
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0.0... |
based on number, titer, and speci ficity of\nautoantibodies as well as age of seroconver-sion and genetic risk (47). Stage 2 includesindividuals with multiple islet autoantibod-ies and dysglycemia. At stage 2 of the dis-ease, there is /C2460% risk by 2 years and\n/C2475% risk within 5 years of developing\nsymptomatic ty... | [
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0.005761... |
symptomatic type 1 diabetes (57,58).\nThe rate of b-cell destruction is quite\nvariable, being rapid in some individuals(particularly but not exclusively in infantsand children) and slow in others (mainlybut not exclusively adults) (46,59). Childrenand adolescents often present with DKAas the first manifestation of the ... | [
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0.0303915... |
and rates in the U.S. have increased dra-\nmatically over the past 20 years (30 –32).\nOthers have modest fasting hyperglycemia\nthat can rapidly change to severe hypergly-cemia and/or DKA with infection or otherstress. Adults may retain suf ficient b-cell\nfunction to prevent DKA for many years;such individuals may hav... | [
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decreased insulin needs for months or\nyears, eventually become dependent oninsulin for survival, and are at risk for DKA(33–35,60,61). At this later stage of thed i s e a s e ,t h e r ei sl i t t l eo rn oi n s u l i ns e c r e -tion, as manifested by low or undetectablelevels of plasma C-peptide. Immune-mediated diab... | [
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0.03793581... |
mon form of diabetes in childhood and\nadolescence, but it can occur at anyage.\nAutoimmune destruction of b-cells has\nmultiple genetic factors and is also re-lated to environmental factors that arestill poorly defi ned. Although individuals | [
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0.030870262533426285,
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0.01481175422668457,
-0.033660851418972015,
0.0146... |
do not typically have obesity when theypresent with type 1 diabetes, obesity isincreasingly common in the general pop-ulation; as such, obesity should not pre-\nclude testing for type 1 diabetes. People | [
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0.011960175819694996,
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0.007390487473458052,
0.03577810153365135,
0.042768802493810654,
-0.10686881095170975,
0.02129... |
clude testing for type 1 diabetes. People\nwith type 1 diabetes are also prone toother autoimmune disorders, such asHashimoto thyroiditis, Graves disease, ce-liac disease, Addison disease, vitiligo, au-toimmune hepatitis, myasthenia gravis,and pernicious anemia (see Section 4,“Comprehensive Medical Evaluation and | [
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0... |
Assessment of Comorbidities” ). Type 1 di-\nabetes can be associated with monogenic\npolyglandular autoimmune syndromes, | [
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0.05... |
polyglandular autoimmune syndromes,\nincluding immune dysregulation, polyen-docrinopathy, enteropathy, and X-linked(IPEX) syndrome, which is an early-onsetsystemic autoimmune, genetic disordercaused by mutation of the forkhead boxprotein 3 (FOXP3 ) gene, and another dis-\norder caused by the autoimmune regula-tor (AIRE... | [
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0.0270050261169672,
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0.038901880383491516,
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0.00... |
Introduction of immunotherapy, specif-\nically checkpoint inhibitors, for cancer\ntreatment has led to unexpected adverse | [
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0.0619935542345047,
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-0.0... |
treatment has led to unexpected adverse\nevents, including immune system activa-tion precipitating autoimmune disease.Fulminant onset of type 1 diabetes canoccur, with DKA and low or undetectablelevels of C-peptide as a marker of endoge-nousb-cell function (64 –66). Fewer thanTable 2.3 —Staging of type 1 diabetes\nStag... | [
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0.008958113379776478,
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0.01099589467048645,
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0.0295748934... |
Stage 1 Stage 2 Stage 3\nCharacteristics /C15Autoimmunity /C15Autoimmunity /C15Autoimmunity\n/C15Normoglycemia /C15Dysglycemia /C15Overt hyperglycemia\n/C15Presymptomatic /C15Presymptomatic /C15Symptomatic\nDiagnostic criteria /C15Multiple islet\nautoantibodies\n/C15No IGT or IFG/C15Islet autoantibodies (usually multip... | [
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... |
/C15Dysglycemia: IFG and/or IGT\n/C15FPG 100 –125 mg/dL (5.6 –6.9 mmol/L)\n/C152-h PG 140 –199 mg/dL (7.8 –11.0 mmol/L)\n/C15A1C 5.7 –6.4% (39 –47 mmol/mol) or $10%\nincrease in A1C/C15Autoantibodies may become absent\n/C15Diabetes by standard criteria | [
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/C15Diabetes by standard criteria\nAdapted from Skyler et al. (40). FPG, fasting plasma glucose; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; 2-h PG, 2-h plasmaglucose. Alternative additional stage 2 diagnostic criteria of 30-, 60-, or 90-min plasma glucose on oral glucose tolerance test $200 mg/dL | [
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($11.1 mmol/L) and con firmatory testing in those aged $18 years have been used in clinical trials (79).S24 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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Type 1 \ndiabetesIndeterminate9\nConsider repeat \nC-peptide at >5 yearsType 2 \ndiabetesGenetic testing for \nmonogenic diabetes \nwhere available6Are there features of \ntype 2 diabetes?5 Test C-peptide4Are there features of monogenic diabetes?3Islet autoantibody negative\n(5-10% of adult-onset type 1 diabetes)Islet ... | [
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(5-10% of adult-onset type 1 diabetes)Islet autoantibody positive\nType 1 diabetes Age\nUnclear classification7\nMake clinical decision as to \nhow person with diabetes \nshould be treated\nTrial of noninsulin therapy may \n8\nConsider C-peptide4 test after \n>3 years duration>35 years\nYes No | [
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8\nConsider C-peptide4 test after \n>3 years duration>35 years\nYes No\n<200 pmol/L 200-600 pmol/L >600 pmol/L <200 pmol/L >200 pmol/L NoTest islet autoantibodies2\n<35 years\nYesAdult with suspected type 1 diabetes1Flow chart for investigation of suspected type 1 diabetes in newly \ndiagnosed adults, based on data fro... | [
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